GALNT14 promotes lung-specific breast cancer metastasis by modulating self-renewal and interaction with the lung microenvironment

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Some polypeptide N-acetyl-galactosaminyltransferases (GALNTs) are associated with cancer, but their function in organ-specific metastasis remains unclear. Here, we report that GALNT14 promotes breast cancer metastasis to the lung by enhancing the initiation of metastatic colonies as well as their subsequent growth into overt metastases. Our results suggest that GALNT14 augments the self-renewal properties of breast cancer cells (BCCs). Furthermore, GALNT14 overcomes the inhibitory effect of lung-derived bone morphogenetic proteins (BMPs) on self-renewal and therefore facilitates metastasis initiation within the lung microenvironment. In addition, GALNT14 supports continuous growth of BCCs in the lung by not only inducing macrophage infiltration but also exploiting macrophage-derived fibroblast growth factors (FGFs). Finally, we identify KRAS-PI3K-c-JUN signalling as an upstream pathway that accounts for the elevated expression of GALNT14 in lung-metastatic BCCs. Collectively, our findings uncover an unprecedented role for GALNT14 in the pulmonary metastasis of breast cancer and elucidate the underlying molecular mechanisms.
Publisher
NATURE PUBLISHING GROUP
Issue Date
2016-12
Language
English
Article Type
Article
Keywords

POLYPEPTIDE N-ACETYLGALACTOSAMINYLTRANSFERASE; O-GLYCOSYLATION; STEM-CELLS; TUMOR REINITIATION; D-GALACTOSAMINE; RNA-SEQ; EXPRESSION; GENES; GROWTH; FAMILY

Citation

NATURE COMMUNICATIONS, v.7

ISSN
2041-1723
DOI
10.1038/ncomms13796
URI
http://hdl.handle.net/10203/220157
Appears in Collection
BS-Journal Papers(저널논문)
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